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首页 » Clin Gas Hepat:研究表明慢性胰腺炎患者大脑皮质厚度会变薄

Clin Gas Hepat:研究表明慢性胰腺炎患者大脑皮质厚度会变薄

来源:爱唯医学网 2012-03-13 10:37

近日,国际著名杂志《临床肠胃病学与肝病学》Clinical Gastroenterology and Hepatology在线刊登了国外研究人员的最新研究成果“Reduced Cortical Thickness of Brain Areas Involved in Pain Processing in Patients With Chronic Pancreatitis,”,文章中,研究者揭示了慢性胰腺炎患者大脑皮质厚度会变薄。

丹麦Aalborg医院/Aarhu大学医院的Jens Brondum Frøkjær博士及其同事报告称,慢性胰腺炎患者大脑内有5个区域的皮质厚度变薄,并且这些区域参与了内脏疼痛感的处理。此外,皮质厚度变薄与患者的疼痛日志评分相关,疼痛最严重者的MRI提示的皮质厚度最薄。

研究者对19例慢性胰腺炎成年患者和15例健康志愿者进行了评价,患者与健康对照者在年龄和性别特征方面均相似。所有受试者在接受头颅MRI扫描之前均完成了1周的疼痛日志。

研究所采用的皮质厚度评估方法是高分辨率三维MRI技术,这与其他研究者在评估肠易激综合征或三叉神经病患者的大脑改变时所采用的技术相同。研究者指出,如今凭借这一新技术可以“准确、稳健、快速地分析皮质厚度”。

结果显示,与对照组相比,胰腺炎患者颅内次级体感觉皮质(Rolandic岛盖)、背外侧前额皮质(额中回)、外侧额皮质(额上回和额下回的眶部)、扣带回皮质中央区和岛叶的皮质厚度变薄。

既往研究表明,次级体感觉皮质激活与患者留意或试图评估疼痛的强度和性质相关;前额皮质是处理内脏疼痛感的中枢,与“疼痛体验的认知方面”有关;额皮质则接收感觉信号,参与疼痛的处理;中扣带回皮质与下丘脑相连,导水管周围灰质被视为是“下行疼痛调节体系的一部分”;岛叶则参与了内脏感觉与运功功能的整合,并且负责将疼痛信号传递至额皮质。

相反,患者与对照者在大脑枕中沟区域的皮质厚度无明显差异,该区域没有参与中枢神经系统的疼痛处理。

结果还显示,这5个区域的皮质变薄与患者的临床疼痛评分相关,但皮质厚度与可能诱发胰腺疼痛的因素无关,比如饮酒过量、合并糖尿病、使用阿片类药物等。此外,有和无持续性胰腺疼痛的患者在皮质厚度方面也没有差异。

以上发现均提示,持续向大脑发送疼痛信号导致了神经矩阵结构重组,研究表明其他以慢性疼痛为特征的疾病也存在这样的变化。研究者指出,皮质变薄“可能是持续的慢性疼痛诱导神经可塑性以及大脑内疼痛矩阵的突触活性增加所致,其中突触活性增加与对抗感受伤害信号的活性降低有关。”此外,该研究也进一步证实了采用MRI测量皮质厚度既快捷又简便,可以作为反映“疼痛体系整体伤害程度和功能障碍”的有效指标之一。

不过,研究者也指出,与胰腺炎相关的其他因素也可能诱导这些脑结构变化。由于该研究没有将不伴腹痛的胰腺炎患者设为对照组,所以无法解答这个问题。(生物谷Bioon.com)

Reduced Cortical Thickness of Brain Areas Involved in Pain Processing in Patients With Chronic Pancreatitis

Jens Brøndum Frøkjær⁎, ‡, , , Stefan A.W. Bouwense§, Søren Schou Olesen⁎, Flemming H. Lundager⁎, Simon F. Eskildsen∥, Harry van Goor§, Oliver H.G. Wilder–Smith¶, Asbjørn Mohr Drewes⁎, ∥

Background & Aims Patients with painful chronic pancreatitis (CP) might have abnormal brain function. We assessed cortical thickness in brain areas involved in visceral pain processing. Methods We analyzed brain morphologies of 19 patients with painful CP and compared them with 15 healthy individuals (controls) by using a 3T magnetic resonance scanner. By using an automated method with surface-based cortical segmentation, we assessed cortical thickness of the primary (SI) and secondary (SII) somatosensory cortex; prefrontal cortex (PFC); frontal cortex (FC); anterior (ACC), mid (MCC), and posterior (PCC) cingulate cortex; and insula. The occipital middle sulcus was used as a control area. The pain score was determined on the basis of the average daily amount of pain during 1 week. Results Compared with controls, patients with CP had reduced overall cortical thickness (P = .0012), without effects of modification for diabetes, alcoholic etiologies, or opioid treatment (all P values >.05). In patients with CP, the cortical thickness was decreased in SII (P = .002, compared with controls), PFC (P = .046), FC (P = .0003), MCC (P = .001), and insula (P = .002). There were no differences in cortical thickness between CP patients and controls in the control area (P = .20), SI (P = .06), ACC (P = .95), or PCC (P = .42). Cortical thickness in the affected areas correlated with pain score (r = 0.47, P = .003). Conclusions In patients with CP, brain areas involved in pain processing have reduced cortical thickness. As a result of long-term, ongoing pain input to the neuromatrix, cortical thickness might serve as a measure for overall pain system dysfunction, as observed in other diseases characterized by chronic pain. Keywords Magnetic Resonance Imaging; Neuroplasticity; Reorganization; Pain Response Abbreviations used in this paper ACC, anterior cingulate cortex; ANOVA, analysis of variance; CP, chronic pancreatitis; FACE, Fast Accurate Cortical Extraction; FC, frontal cortex; MCC, mid cingulate cortex; MRI, magnetic resonance imaging; PCC, posterior cingulate cortex; PFC, prefrontal cortex; ROI, region of interest; SI, primary somatosensory cortex; SII, secondary somatosensory cortex

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